Realization path and connotation of the Healthy China strategy: macroscopic perspective of dietary structure and the entry of individual health consciousness.

BACKGROUND: Dietary rationality and health concept have certain influence on individual health level. This study aims to explore the characteristics and existing problems of Chinese residents' health behaviors from both macro and micro perspectives, and explore the feasibility and realization path of Healthy China strategy. METHODS: We utilized regression models to evaluate the correlation between diet and the risk of disease causes of death. By use of the linear regression analysis model, we distinguished the impact of each dimension on health literacy index at the individual level. Then, we explored the influential factors of the diet health index using the binary logit regression model. RESULTS: Increased consumption of animal-derived foods in China has contributed to the burden of non-communicable diseases. The individuals' health awareness is still weak, and the health literacy index is greatly affected by the diet, while the individual gender and age are positively correlated with the diet health index, and the individual body mass index (BMI) level is negatively correlated with the diet health index. CONCLUSIONS: This study provided a comprehensive understanding of existing problems of Chinese residents' health behaviors. We have proposed a path model for the implementation of the Healthy China strategy from the perspectives of "diet health, physical health, conceptual health and environmental health," which is also a great contribution to the world.

Inhibition of miR-146a-5p and miR-8114 in Insulin-Secreting Cells Contributes to the Protection of Melatonin against Stearic Acid-Induced Cellular Senescence by Targeting Mafa.

BACKGRUOUND: Chronic exposure to elevated levels of saturated fatty acids results in pancreatic ß-cell senescence. However, targets and effective agents for preventing stearic acid-induced ß-cell senescence are still lacking. Although melatonin administration can protect ß-cells against lipotoxicity through anti-senescence processes, the precise underlying mechanisms still need to be explored. Therefore, we investigated the anti-senescence effect of melatonin on stearic acid-treated mouse ß-cells and elucidated the possible role of microRNAs in this process. METHODS: ß-Cell senescence was identified by measuring the expression of senescence-related genes and senescence-associated ß-galactosidase staining. Gain- and loss-of-function approaches were used to investigate the involvement of microRNAs in stearic acid-evoked ß-cell senescence and dysfunction. Bioinformatics analyses and luciferase reporter activity assays were applied to predict the direct targets of microRNAs. RESULTS: Long-term exposure to a high concentration of stearic acid-induced senescence and upregulated miR-146a-5p and miR- 8114 expression in both mouse islets and ß-TC6 cell lines. Melatonin effectively suppressed this process and reduced the levels of these two miRNAs. A remarkable reversibility of stearic acid-induced ß-cell senescence and dysfunction was observed after silencing miR-146a-5p and miR-8114. Moreover, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (Mafa) was verified as a direct target of miR-146a-5p and miR-8114. Melatonin also significantly ameliorated senescence and dysfunction in miR-146a-5pand miR-8114-transfected ß-cells. CONCLUSION: These data demonstrate that melatonin protects against stearic acid-induced ß-cell senescence by inhibiting miR-146a- 5p and miR-8114 and upregulating Mafa expression. This not only provides novel targets for preventing stearic acid-induced ß-cell dysfunction, but also points to melatonin as a promising drug to combat type 2 diabetes progression.

Overexpression of miR-297b-5p protects against stearic acid-induced pancreatic ß-cell apoptosis by targeting LATS2.

Chronic exposure to high concentrations of stearic acid (C18:0) can result in ß-cell dysfunction, leading to development of type 2 diabetes. However, the molecular mechanisms underlying the destructive effects of stearic acid on ß-cells remain largely unknown. In this study, we aimed to investigate the role of miR-297b-5p on stearic acid-induced ß-cell apoptosis. Differential expression of microRNAs (miRNAs) was assessed in a ß-TC6 cell line exposed to stearic acid, palmitic acid, or a normal culture medium by high-throughput sequencing. The apoptosis rate was measured by flow cytometry after miR-297b-5p mimic/inhibitor transfection, and large-tumor suppressor kinase 2 (LATS2) was identified as a target of miR-297b-5p using a luciferase activity assay. In vivo, C57BL/6 mice were fed with normal and high-stearic-acid diet, respectively. Mouse islets were used for similar identification of miR-297b-5p and Lats2 in ß-TC6 cell. We selected two differentially expressed miRNAs in stearic acid compared with those in the palmitic acid and control groups. miR-297b-5p expression was significantly lower in ß-TC6 cells and mouse islets in stearic acid than in control group. Upregulation of miR-297b-5p alleviated the stearic acid-induced cell apoptosis and reduction in insulin secretion by inhibiting Lats2 expression in vitro. Meanwhile, silencing Lats2 significantly reversed the stearic acid-stimulated ß-cell dysfunction in both ß-TC6 cells and islets. Our findings indicate a suppressive role for miR-297b-5p in stearic acid-induced ß-cell apoptosis, which may reveal a potential target for the treatment of ß-cell dysfunction in the pathogenesis of type 2 diabetes.